ライフサイエンスコーパス: nephrogenic

1 classified as embryonal adenomas and one as nephrogenic adenofibroma.

2 formation in transparent larvae showed that nephrogenic aggregates form by the coalescence of multip

3 from NCAM1(+) progenitors, and recapitulate nephrogenic and ureteric bud lineages.

4 s, these NPCs are integrated into a specific nephrogenic area of the kidney and contain slow-cycling

5 6.TC mice produce high titers of antinuclear nephrogenic autoantibodies and a highly penetrant glomer

6 tus are crucial determinants of the kidney's nephrogenic capacity.

7 athogenic SMAD2 variants in podocytogenesis, nephrogenic cell lineage specification and glomerular fi

8 7) show that targeted Pax2 deletion converts nephrogenic cells to the stromogenic path, suggesting th

9 ion of Hox and Wnt signaling genes in mutant nephrogenic cells.

10 MM cells than in intact mesenchyme, and the nephrogenic competence of transduced drMM progenitor cel

11 termediate mesoderm at the caudal end of the nephrogenic cord.

12 PP2A was found predominately in the nephrogenic cortex and particularly in the developing gl

13 ng kidney development and its mapping to the nephrogenic cortex, developing glomeruli, and tubules su

14 ry, Tie-2 was detected in capillaries of the nephrogenic cortex, glomerular tufts, cortical interstit

15 elic KO mutations of the target gene induced nephrogenic defects; however, biallelic mutations involv

16 erlying aetiology and differs in central DI, nephrogenic DI and primary polydipsia.

17 Central and nephrogenic DI are usually acquired, but genetic causes

18 Central or nephrogenic DI must be differentiated from primary polyd

19 pituitary gland or the hypothalamus, whereas nephrogenic DI results from resistance to AVP in the kid

20 To reduce lithium-induced nephrogenic diabetes insipidus (lithium-NDI), patients w

21 aquaporin-2 (AQP2) point mutants that cause nephrogenic diabetes insipidus (NDI) are retained in the

22 Animal models of a variety of acquired nephrogenic diabetes insipidus (NDI) disorders have iden

23 Congenital nephrogenic diabetes insipidus (NDI) is a rare disease c

24 Nephrogenic diabetes insipidus (NDI) is caused by impair

25 Hereditary non-X-linked nephrogenic diabetes insipidus (NDI) is caused by mutati

26 wn in a variety of animal models of acquired nephrogenic diabetes insipidus (NDI) that loss of the aq

27 A Mexican family with partial congenital nephrogenic diabetes insipidus (NDI) that resulted from

28 n-2 (AQP2) mutations that cause non-X-linked nephrogenic diabetes insipidus (NDI) were characterized

29 20% of patients treated with lithium develop nephrogenic diabetes insipidus (NDI), a disorder charact

30 fect in urinary concentrating ability, i.e., nephrogenic diabetes insipidus (NDI), but the molecular

31 ep in generating a transgenic mouse model of nephrogenic diabetes insipidus (NDI), we have analyzed t

32 tein expression in mice with lithium-induced nephrogenic diabetes insipidus (NDI).

33 pressin and defective trafficking results in nephrogenic diabetes insipidus (NDI).

34 r processing can produce autosomal recessive nephrogenic diabetes insipidus (NDI).

35 Congenital nephrogenic diabetes insipidus (NDI; also known as argin

36 a nonsense mutation known to cause X-linked nephrogenic diabetes insipidus (XNDI) in humans (Glu242s

37 X-linked nephrogenic diabetes insipidus (XNDI) is a severe kidney

38 MIP underlie an autosomal recessive form of nephrogenic diabetes insipidus and absence of the Colton

39 -of-function mutations in aquaporins include nephrogenic diabetes insipidus and congenital cataracts.

40 nstay treatment for bipolar disorder, causes nephrogenic diabetes insipidus and hypercalcemia in abou

41 cost of severe renal side effects, including nephrogenic diabetes insipidus and rarely, ESRD.

42 these results identify a novel mechanism of nephrogenic diabetes insipidus and uncover a role of SOC

43 Finally, renal distal tubular acidosis or nephrogenic diabetes insipidus can be caused by autoanti

44 Other features included nephrogenic diabetes insipidus in 87% and hypertension i

45 children, and distal tubular toxicity caused nephrogenic diabetes insipidus in one.

46 The most common cause of hereditary nephrogenic diabetes insipidus is a nonfunctional vasopr

47 This nephrogenic diabetes insipidus leads to dehydration and

48 chronic experimental iron overload leads to nephrogenic diabetes insipidus marked by AVP-resistant u

49 Our findings establish a form of nephrogenic diabetes insipidus produced by impaired wate

50 The nephrogenic diabetes insipidus symptoms and the absence

51 ceptors known to be responsible for X-linked nephrogenic diabetes insipidus were used as model system

52 hat Foxa1(-/-) mice represent a new model of nephrogenic diabetes insipidus with unique molecular eti

53 forms of diabetes insipidus (e.g., X-linked nephrogenic diabetes insipidus) in which the kidney resp

54 familiar diseases such as Gaucher's disease, nephrogenic diabetes insipidus, and Creutzfeldt-Jakob di

55 e for retinitis pigmentosa, color blindness, nephrogenic diabetes insipidus, familial ACTH resistance

56 hium, a potent inhibitor of GSK3beta, causes nephrogenic diabetes insipidus, GSK3beta may play a cruc

57 ion R137H, which is associated with familial nephrogenic diabetes insipidus, induces constitutive arr

58 The mice had severe polyuria and nephrogenic diabetes insipidus, potentially due to great

59 have shown that a molecular determinant for nephrogenic diabetes insipidus, the vasopressin receptor

60 with tolvaptan, a VR2 blocker that causes a nephrogenic diabetes insipidus-like excessive loss of hy

61 VP, a vasopressin analog), characteristic of nephrogenic diabetes insipidus.

62 nt selected alleles responsible for X-linked nephrogenic diabetes insipidus.

63 otypes--ranging from congenital cataracts to nephrogenic diabetes insipidus.

64 deletion in mice produces distinct forms of nephrogenic diabetes insipidus.

65 ility; mutations or downregulation can cause nephrogenic diabetes insipidus.

66 and the responses underlying lithium-induced nephrogenic diabetes insipidus.

67 were compatible with a diagnosis of partial nephrogenic diabetes insipidus.

68 in renal handling of water in health and in nephrogenic diabetes insipidus.

69 and trafficking, the absence of which causes nephrogenic diabetes insipidus.

70 alcitonin has a potential therapeutic use in nephrogenic diabetes insipidus.

71 vasopressin 2 receptor and aquaporin 2 cause nephrogenic diabetes insipidus; however, expression of t

72 pressor complexes to antagonize Wnt-directed nephrogenic differentiation.

73 Accordingly, inhibiting LRPPRC negates the nephrogenic effects of SAM and METTL3.

74 tive mastermind-like (dnMaml) peptide in the nephrogenic epithelia from after the s-shaped body forma

75 Key nephrogenic factors are distinguished by strong correlat

76 bodies that are cultured in the presence of nephrogenic factors can respond to inductive signals and

77 ding to positional information that controls nephrogenic fate.

78 Nephrogenic fibrosing dermopathy (NFD) is a newly recogn

79 Nephrogenic fibrosing dermopathy (NFD) is a newly recogn

80 Nephrogenic systemic fibrosis, also known as nephrogenic fibrosing dermopathy, was first documented i

81 s possible to begin to understand the normal nephrogenic function of the wild-type proteins and under

82 LS-FMD induced modulation of a nephrogenic gene program, resembling renal developmental

83 This study used a combination of nephrogenic growth factors to differentiate ES cells int

84 ggest that activation of beta-catenin in the nephrogenic lineage results in loss of nephron progenito

85 The nephrogenic mesenchymal lineage in fgfr2(UB-/-) mice dev

86 Although enhancers for pigmented epithelium, nephrogenic mesenchyme and apical ectodermal ridge are d

87 re/+) allele leads to disorganization of the nephrogenic mesenchyme and impairment of mesenchyme indu

88 pulation of cells expressing markers of both nephrogenic mesenchyme and peripheral stroma.

89 reveals mechanisms regulating persistence of nephrogenic mesenchyme and provides a rationale for ther

90 data suggest a novel interaction between the nephrogenic mesenchyme and stromal progenitor cell popul

91 n the recruitment and/or organization of the nephrogenic mesenchyme at early time-points of kidney de

92 t are a likely result of progressive loss of nephrogenic mesenchyme by apoptosis.

93 le is known about the mechanism by which the nephrogenic mesenchyme cell population is maintained at

94 ded by two distinct mesenchymal populations: nephrogenic mesenchyme derived from the intermediate mes

95 null mesenchyme cells at E11.5 show that the nephrogenic mesenchyme does not aggregate tightly around

96 on is inappropriately maintained in anterior nephrogenic mesenchyme in these mutants.

97 conclude that the failure of recruitment of nephrogenic mesenchyme leaves a primitive population of

98 show that induction and condensation of the nephrogenic mesenchyme occurs normally in mutant.

99 bservation that the ureteric bud induced the nephrogenic mesenchyme to undergo tubulogenesis.

100 1, Pax2, and Wt1, are all down-regulated and nephrogenic mesenchyme undergoes massive apoptosis, resu

101 By contrast, removal of Smad4 in nephrogenic mesenchyme using the Bmp7(cre/+) allele lead

102 We found that the nephrogenic mesenchyme, which is required for continued

103 ng generated from a stem-cell population-the nephrogenic mesenchyme-in response to signals emanating

104 the SLIT2/ROBO2 signal is transduced in the nephrogenic mesenchyme.

105 c lineage mapping of the collecting duct and nephrogenic mesenchyme.

106 in response to GDNF secreted by the adjacent nephrogenic mesenchyme.

107 ct with Pax2 and Eya1, factors important for nephrogenic mesoderm specification, to directly regulate

108 al Wnt signalling is not active in the early nephrogenic metanephric mesenchyme, but instead provide

109 correlating with disturbed expression of key nephrogenic molecules.

110 cts regionally induced commitment within the nephrogenic niche in mice.

111 eteric bud tip) transcripts to determine the nephrogenic niche postnatal lifespan.

112 uggest that studies of arcading in postnatal nephrogenic niche should be performed within the first 5

113 We performed 3D rendering of the nephrogenic niche to assess for PBN, and supplemented th

114 hy, three-dimensional reconstructions of the nephrogenic niche, and transcriptome and DNA methylation

115 at heterozygous mutant expression in Six2(+) nephrogenic or Foxd1(+) stromal lineages leads to severe

116 o determine whether the DI was of central or nephrogenic origin, we examined the responsiveness of th

117 The nephrogenic pattern of Ang-2 was documented in a mouse s

118 protein-energy malnutrition in sheep blunts nephrogenic potential in the 0.44 gestation (65 days ges

119 enomic stability, molecular homogeneity, and nephrogenic potential in vitro, ex vivo, and in vivo.

120 Elements that direct Pax2 expression to nephrogenic precursor cells must be responding to positi

121 tirety of organogenesis, focusing on two key nephrogenic progenitor populations: the ureteric epithel

122 kidney development in mice markedly expands nephrogenic progenitors by blocking their final wave of

123 eta-catenin (Ctnnb1)-driven, transcriptional nephrogenic program and the mesenchymal to epithelial tr

124 rowth, genetic increase of GDNF prolongs the nephrogenic program beyond its normal cessation.

125 The spatially resolved nephrogenic program made available through the Human Nep

126 rmissive environment for continuation of the nephrogenic program, as demonstrated by morphologically

127 ene targets poised for rapid initiation of a nephrogenic program.

128 nal protein maps on anatomical models of the nephrogenic program.

129 Nephrogenic programming was dependent on Lef/Tcf factors

130 directs expression of a lacZ reporter to the nephrogenic region and the midbrain-hindbrain junction i

131 nificantly attenuates lacZ expression in the nephrogenic region but not in the midbrain-hindbrain reg

132 y (FH) tumors (100% and 92%), and intralobar nephrogenic rests (ILNR; 77% and 22%) all differed.

133 significantly associated with both perilobar nephrogenic rests and 11p15 imprinting aberrations.

134 Thirty-four Wilms' tumors with nephrogenic rests and/or areas of anaplasia were microdi

135 Intralobar and perilobar nephrogenic rests are known to have different biological

136 Nephrogenic rests are precursor lesions associated with

137 blastoma is believed to arise from embryonic nephrogenic rests of multipotent cells that fail to term

138 Nephrogenic rests show increases in methylation levels r

139 n of abnormally persistent renal stem cells (nephrogenic rests) which retain embryonic differentiatio

140 ncreased risk was observed for patients with nephrogenic rests, bilateral tumors, history of secondar

141 n pathway response and leads to precancerous nephrogenic rests.

142 ve a high prevalence of precursor intralobar nephrogenic rests.

143 analysis of Wilms' tumour precursor lesions, nephrogenic rests.

144 Amid mounting concerns about nephrogenic sclerosis and gadolinium deposition in the b

145 tubule dedifferentiation, with a pronounced nephrogenic signature represented by Sox4 and Cd24a.

146 g-term kidney injuries activated a prominent nephrogenic signature, including Sox4 and Hox gene eleva

147 mouse revealed a transient, mouse-like, pre-nephrogenic, Six1 regulatory pattern.

148 tromogenic stem cells and [Six2(+), Pax2(+)] nephrogenic stem cells.

149 zation of mutant receptors for patients with nephrogenic syndrome of inappropriate antidiuresis becau

150 ding the V2 vasopressin receptor (V2R) cause nephrogenic syndrome of inappropriate antidiuresis.

151 like clinical picture, which we have termed "nephrogenic syndrome of inappropriate antidiuresis."

152 Background Although nephrogenic systemic fibrosis (NSF) affects the use of g

153 The risk for nephrogenic systemic fibrosis (NSF) after exposure to ne

154 st agents for hypersensitivity reactions and nephrogenic systemic fibrosis (NSF) but had lower confid

155 Background The risk of nephrogenic systemic fibrosis (NSF) following administra

156 The risk of nephrogenic systemic fibrosis (NSF) from group II GBCM i

157 bodies were thought to be pathognomonic for nephrogenic systemic fibrosis (NSF) in the setting of ch

158 Nephrogenic systemic fibrosis (NSF) is a fibrosing skin

159 Nephrogenic systemic fibrosis (NSF) is a rapidly progres

160 Nephrogenic systemic fibrosis (NSF) is a severe fibrosin

161 Nephrogenic systemic fibrosis (NSF) is associated with g

162 icates that there are limited data regarding nephrogenic systemic fibrosis (NSF) risk, but there are

163 m patients with systemic sclerosis (SSc) and nephrogenic systemic fibrosis (NSF) was performed to ide

164 sented as a novel means for the diagnosis of nephrogenic systemic fibrosis (NSF), a rare disease occu

165 disease, have been strongly associated with nephrogenic systemic fibrosis (NSF), a severe systemic f

166 ew data in 13 patients with biopsy-confirmed nephrogenic systemic fibrosis (NSF), assess the associat

167 e a small risk of adverse effects, including nephrogenic systemic fibrosis (NSF), the untreatable con

168 mpaired kidney function and the incidence of nephrogenic systemic fibrosis (NSF).

169 eir product labeling to describe the risk of nephrogenic systemic fibrosis (NSF).

170 connective tissue or skin disease resembling nephrogenic systemic fibrosis (NSF-like) and a broader s

171 ction, but there is also a risk of producing nephrogenic systemic fibrosis and cerebral deposits of u

172 imuli may participate in the pathogenesis of nephrogenic systemic fibrosis and of other fibrotic diso

173 Clinical reports support the evidence of nephrogenic systemic fibrosis as a systemic disease and

174 Gd(3+) and potential side effects including nephrogenic systemic fibrosis have led to the search for

175 dolinium-based contrast agents are linked to nephrogenic systemic fibrosis in patients with renal ins

176 lain their causal role in the development of nephrogenic systemic fibrosis in renally impaired patien

177 n Gadoxetic acid may be safe with respect to nephrogenic systemic fibrosis in this patient population

178 Nephrogenic systemic fibrosis is a new disorder reported

179 The pathology of nephrogenic systemic fibrosis is characterized by abnorm

180 Clinical awareness of nephrogenic systemic fibrosis is still emerging and futu

181 o uniformly effective interventions to treat nephrogenic systemic fibrosis other than successful rena

182 lls in the fibrotic and calcified tissues of nephrogenic systemic fibrosis patients.

183 While a specific cause of nephrogenic systemic fibrosis remains to be established,

184 pe and function relevant to the pathology of nephrogenic systemic fibrosis using immunofluorescence,

185 udies are scant; therefore, a mouse model of nephrogenic systemic fibrosis was established.

186 ased contrast agents in patients at risk for nephrogenic systemic fibrosis was recently shown to avoi

187 cts) and from lesional skin of patients with nephrogenic systemic fibrosis were exposed to a range of

188 No cases of nephrogenic systemic fibrosis were noted.

189 Although 639 patients with biopsy-confirmed nephrogenic systemic fibrosis were reported, only seven

190 Med database was searched by using the term "Nephrogenic systemic fibrosis" from January 2000 to Febr

191 Nephrogenic systemic fibrosis, also known as nephrogenic

192 e recent association of this lanthanide with nephrogenic systemic fibrosis, an untreatable disease, h

193 We also examined tissues from patients with nephrogenic systemic fibrosis, using IHC to identify the

194 g that gadoxetate disodium does not incite a nephrogenic systemic fibrosis-like fibrotic change in th

195 of a sometimes fatal condition in patients, nephrogenic systemic fibrosis.

196 plays a critical role in the pathogenesis of nephrogenic systemic fibrosis.

197 , cases were analyzed for the development of nephrogenic systemic fibrosis.

198 ical and pathologic findings consistent with nephrogenic systemic fibrosis.

199 None of the neonates developed nephrogenic systemic fibrosis.

200 ystemic fibrosis and ectopic ossification in nephrogenic systemic fibrosis.

201 ts with severe renal dysfunction at risk for nephrogenic systemic fibrosis.

202 Nephrogenic systemic sibrosis is a progressive disorder

203 ve repair evidenced by dedifferentiation and nephrogenic transcriptional signatures.

204 In particular, postnatal maturation of the nephrogenic zone (NZ) is defective.

205 tion and increased apoptosis of cells in the nephrogenic zone and a progressive decrease in the numbe

206 -dysplastic kidneys, patchy depletion of the nephrogenic zone and pockets of superficially placed, ec

207 expressed in the developing nephrons in the nephrogenic zone and ureteric bud branches, where the si

208 IF-2alpha mRNAs were highly expressed in the nephrogenic zone of newborn kidney cortex and in the med

209 main protein Cux1 is highly expressed in the nephrogenic zone of the developing kidney where it funct

210 Dnmt1 and Dnmt3a are highly enriched in the nephrogenic zone of the developing kidneys.

211 reduced numbers of nephrons and lacking the nephrogenic zone where new nephrons are continuously add

212 Histomorphometry indicated decreased nephrogenic zone width (p = 0.039) with increased number

213 epletion, and altered Jag1 expression in the nephrogenic zone, consistent with premature differentiat

214 apoptosis and decreasing angiogenesis in the nephrogenic zone, effects that were more marked in male

215 esenchyme (MM), particularly in the cortical nephrogenic zone, which provides the progenitors for rec

216 ed incorporation into blastemal cells of the nephrogenic zone.

217 ed regions of mesenchymal condensates in the nephrogenic zone.

218 ing kidney with expression restricted to the nephrogenic zone.

219 to defective UB branching and underdeveloped nephrogenic zone.